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Qishen Yiqi Dripping Pills Combined with Exosomes Alleviate Myocardial I/R Injury by Regulating Macrophage
Weibin Qin1, Weizhi Tang1, Meng Wang2
1Cardiovascular Medicine II, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530000, Guangxi, China
Introduction:
To investigate the protective mechanism of Qishen Yiqi Dropping Pills (Qishen) and its key active ingredients in combination with exosomes from bone marrow mesenchymal stem cells (BMSCs) against myocardial ischemia/reperfusion (I/R) injury.
Methods:
Infarct area was assessed by Evan's Blue/TTC double staining, myocardial apoptosis was analyzed by TUNEL staining, ATP content and NAD+/NADH ratio were detected biochemically, macrophage phenotype of myocardial tissues was detected by flow cytometry, activation of the mTOR/PI3K/Akt pathway was detected by Western blotting, and miR-155-5p expression was detected by qRT-PCR. 155-5p expression. Exo were given to identify the M1/M2 phenotypic transition by immunofluorescence, and the molecular mechanism was verified as in the in vivo experiments.
Results:
Compared with the model group, the Qishen, ginsenoside, and Exo group significantly reduced the infarcted area of the heart and promoted M2 and M2 phenotypic conversion, promoted M2- type macrophage infiltration, up-regulated the p-Akt/Akt ratio, and inhibited the expression of miR- 155-5p, but the combination therapy group did not show a synergistic effect, but the above protective effects were significantly weakened by the removal of macrophages. Ginsenoside and Exo synergistically promoted M2 polarization, activated the mTOR/PI3K/Akt pathway and upregulated miR-155-5p expression.
Discussion:
Qishen, particularly its active component ginsenoside, synergizes with BMSC-Exo to alleviate myocardial I/R injury by modulating macrophage polarization via the miR-155- 5p/mTOR/PI3K/Akt signaling axis.
Conclusion:
Qishen synergistically regulates the miR-155-5p/mTOR/PI3K/Akt signaling axis through ginsenoside components in BMSCs exosomes, promoting macrophage polarization toward M2-type, improving myocardial energy metabolism and attenuating I/R injury, and this protective effect is macrophage-dependent.

